title: Nigral inhibition of GABAergic neurons in mouse superior colliculus.
abstract: The current dominant concept for the control of saccadic eye movements by the basal ganglia is that release from tonic GABAergic inhibition by the substantia nigra pars reticulata (SNr) triggers burst firings of intermediate gray layer (SGI) neurons in the superior colliculus (SC) to allow saccade initiation. This hypothesis is based on the assumption that SNr cells inhibit excitatory projection neurons in the SGI. Here we show that nigrotectal fibers are connected to local GABAergic neurons in the SGI with a similar frequency to non-GABAergic neurons. This was accomplished by applying neuroanatomical tracing and slice electrophysiological experiments in GAD67-green fluorescent protein (GFP) knock-in mice, in which GABAergic neurons specifically express GFP. We also found that GABA(A), but not GABA(B), receptors subserve nigrotectal transmission. The present results revealed a novel aspect on the role of the basal ganglia in the control of saccades, e.g., the SNr not only regulates burst initiation but also modulates the spatiotemporal properties of premotor neurons via connections to local GABAergic neurons in the SC.
authors.affiliation: Department of Developmental Physiology, National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8585, Japan. kaneda@nips.ac.jp
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Kaneda
authors.forename: Kaoru
authors.initials: K
authors.lastname: Isa
authors.forename: Yuchio
authors.initials: Y
authors.lastname: Yanagawa
authors.forename: Tadashi
authors.initials: T
authors.lastname: Isa
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D000818:Animals; D000831:Animals, Newborn; D001710:Biotin / Q000031:analogs & derivatives / Q000378:metabolism; D003911:Dextrans / Q000378:metabolism; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005968:Glutamate Decarboxylase / Q000235:genetics; D049452:Green Fluorescent Proteins / Q000096:biosynthesis; D066298:In Vitro Techniques; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D008239:Lysine / Q000031:analogs & derivatives / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D051379:Mice; D008822:Mice, Transgenic; D009412:Nerve Fibers / Q000502:physiology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques / Q000379:methods; D013378:Substantia Nigra / Q000502:physiology*; D013477:Superior Colliculi / Q000166:cytology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D003911:Dextrans; D018691:Excitatory Amino Acid Antagonists; C076397:biotinylated dextran amine; D049452:Green Fluorescent Proteins; D005680:gamma-Aminobutyric Acid; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D001710:Biotin; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1; C013411:biocytin; D008239:Lysine